The initial step in the activation of the allergic airway response is the ability of inhaled allergen to activate IgE molecules on the pulmonary mast cell to release stored mediators and generate synthesis of new products, which can acutely contract airway smooth muscle. The mast cell also is capable of generating a variety of cytokines, which, in turn, can cause persistence and progression of the allergic response by furthering the underlying inflammation. In addition to mast cell activation, inhaled allergens are capable of stimulating resident lymphocytes in the lung. It is proposed that these allergen-responsive lymphocytes belong to a subpopulation of T helper cells (Th2), which are capable of generating a variety of cytokines, i.e. interleukin (IL)-4, IL-5, and IL-13. These Th2 cytokines can activate the local inflammatory response and can also serve to initiate events outside the lung, which can then further promote the persistence of the allergic inflammatory response.